I am forwarding a slightly modified version of my previous post with the same 
title which was rejected by the FIS list due to the heavy attachments. The most 
significant addition is written in green.  The removed attachments are now 
replaced by their web addresses from which they can be downloaded free of 



From: Sungchul Ji
Sent: Thursday, April 19, 2018 11:02 AM
Cc: Sergey Petoukhov; dani...@shirasawa-acl.net; John Stuart Reid; sayer ji; 
sji.confor...@gmail.com; x...@chemistry.harvard.edu; 
sbur...@proteomics.rutgers.edu; n...@princeton.edu
Subject: The 'Shirasawa phenomenon' or the 'Shirasawa effect"

Hi FISers,

In 2003, Takuji Shirasawa and his coworkers [1] found that mutating certain 
amino acids in the hemoglobin molecule (Hb) in mice produced the following 

(1) increase O_2 consumption and CO_2 production,

(2) the conversion of the muscle histology from a fast glycolytic to a fast 
oxidative type,

(3) a mild anemia, and

(4) faster running speed.

In other words, Shirasawa et al provided a concrete example of molecular 
changes (e.g., amino acid mutations in Hb)  leading to (or associated with) 
macroscopic physiological changes in whole animals (e.g., anemia,  running 
behavior, etc.).  For the convenience of discussions, I am taking the liberty 
of referring to this finding as the "Shirasawa et al. phenomenon/effect" or, 
more briefly, the "Shirasawa phenomenon/effect" which may be viewed as the 
macroscopic version of the Bohr effect [2].

The 'Shirasawa phenomenon/effect' is not limited to hemoglobin.  There are now 
many similar phenomena found in the fields of voltage-gated ion channels, i.e., 
molecular changes in the amino acid sequences of ion channel proteins leading 
to (or associated with) macroscopic effects on the human body called diseases 

Although the current tendency among practicing molecular biologists and 
biophysicists would be to explain away what is here called the Shirasawa 
phenomenon in terms of the microscopic changes "causing" the macroscopic 
phenomenon in a 1:1 basis, another possibility is that the microscopic changes 
"cause" a set of other microscopic changes at the DNA molecular level which in 
turn cause a set of macroscopic changes", in a many-to-many fashion.

Current trend:  Microscopic change (Hb mutation) --------->  Macroscopic change 
1 (Oxygen affinity change of blood) ---------> Macroscopic change 2 (O_2 
 anemia, running behavior)

Althernative mechanism:  Microscopic change 1 (Hb mutation) -------> 
Microscopic change 2 (Changes in the standing waves in DNA) -------> Multiple 
macroscopic changes (O_2 metabolism, anemia, muscle cell histological changes).

The alternative mechanism proposed here seems to me to be more consistent with 
the newly emerging models of molecular genetics [4] and single-molecule 
enzymology [5, 6].

Since the 'Shirasawa phenomenon/effect' evidently implicates information 
transfer from the microscale to the macroscale, it may be of interest to many 
information theoreticians in this group.   If you have any questions, comments, 
or suggestions, please let me know.

All the best.



   [1] Shirasawa, T., et al. (2003).  Oxygen Affinity of Hemoglboin Regulaters 
O_2 Comsumtion, Metabolism, and Physical Activity.  J. Biol. Chem. 278(7): 
5035-5043.  PDF at http://www.jbc.org/content/278/7/5035.full.pdf

   [2] The Bohr effect.  https://en.wikipedia.org/wiki/Bohr_effect
   [3] Huang W, Liu M, S Yan F, Yan N. (2017).  Structure-based assessment of 
disease-related mutations in human voltage-gated sodium 
 Protein Cell. 8(6):401-438. PDF at https://www.ncbi.nlm.nih.gov/pubmed/28150151

   [4] Petoukhov, S. V. (2016).  The system-resonance approach in modeling 
genetic structures. BioSystems 139: 1–11. PDF at 

   [5] Lu, H. P., Xun, L. and Xie, X. S. (1998) Single-Molecule Enzymatic 
Dynamics. Science 282:1877-1882.  PDF at 
   [6] Ji, S. (2017). RASER Model of Single-Molecule Enzyme Catalysis and Its 
Application to the Ribosome Structure and Function. Arch Mol. Med & Gen 1:104. 
PDF at http://hendun.org/journals/AMMG/PDF/AMMG-18-1-104.pdf

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